indication

For the short-term treatment (up to 8 weeks) of active duodenal ulcer, as well as maintenance therapy for duodenal ulcer patients at reduced dosage (1 gram twice a day) after healing of acute ulcers. Also used for the short-term treatment of gastric ulcer.

pharmacology

Sucralfate is a prescription medication used to treat peptic ulcers. The current clinical uses of sucralfate are limited. It is effective for the healing of duodenal ulcers, but it is not frequently used for this since more effective drugs (e.g. proton pump inhibitors) have been developed. Although the mechanism of sucralfate's ability to accelerate healing of duodenal ulcers remains to be fully defined, it is known that it exerts its effect through a local, rather than systemic, action. Chemically, sucralfate is a complex of the disaccharide sugar, sucrose, combined with sulfate and aluminum. In acidic solutions (e.g. gastric acid) it forms a thick paste that has a strong negative charge.

mechanism of action

Although sucralfate's mechanism is not entirely understood, there are several factors that most likely contribute to its action. Sucralfate, with its strong negative charge, binds to exposed positively-charged proteins at the base of ulcers. In this way, it coats the ulcer and forms a physical barrier that protects the ulcer surface from further injury by acid and pepsin. It directly inhibits pepsin (an enzyme that breaks apart proteins) in the presence of stomach acid and binds bile salts coming from the liver via the bile thus protecting the stomach lining from injury caused by the bile acids. Sucralfate may increase prostaglandin production. Prostaglandins are known to protect the lining of the stomach and may also bind epithelial growth factor and fibroblast growth factor, both of which enhance the growth and repair mechanism of the stomach lining.

toxicity

Acute oral toxicity (LD₅₀) in mice is >8000 mg/kg. There is limited experience in humans with overdosage of sucralfate. Sucralfate is only minimally absorbed from the gastrointestinal tract and thus risks associated with acute overdosage should be minimal. In rare reports describing sucralfate overdose, most patients remained asymptomatic.

absorption

Minimally absorbed from the gastrointestinal tract (up to 5% of the disaccharide component and less than 0.02% of aluminum).

half life

Not known.

route of elimination

The small amounts of the sulfated disaccharide that are absorbed are excreted primarily in the urine.

drug interactions

Calcipotriol: Vitamin D Analogs may increase the serum concentration of Sucralfate. Specifically, the absorption of aluminum from sucralfate may be increased, leading to an increase in the serum aluminum concentration. Avoid chronic and/or excessive use of aluminum and aluminum-containing products (such as sucralfate) in patients who are also taking vitamin D analogs. Any patients consuming such a combination should be monitored closely for aluminum status and signs/symptoms of aluminum-related toxicities.

Cholecalciferol: Vitamin D analogs such as cholecalciferol may increase the serum concentration of sucralfate. Specifically, the absorption of aluminum from sucralfate may be increased, leading to an increase in the serum aluminum concentration. Avoid chronic and/or excessive use of aluminum and aluminum-containing products (such as sucralfate) in patients who are also taking vitamin D analogs. Any patients consuming such a combination should be monitored closely for aluminum status and signs/symptoms of aluminum-related toxicities.

Ciprofloxacin: Formation of non-absorbable complexes

Clodronate: Formation of non-absorbable complexes

Etidronic acid: Formation of non-absorbable complexes

Fosphenytoin: Sucralfate decreases the effect of hydantoin

Gatifloxacin: Formation of non-absorbable complexes

Gemifloxacin: Formation of non-absorbable complexes

Grepafloxacin: Formation of non-absorbable complexes

Ibandronate: Formation of non absorbable complexes

Itraconazole: Sucralfate may decrease the absorption of itraconazole.

Ketoconazole: Sucralfate may decrease the absorption of ketoconazole.

Lansoprazole: Sucralfate decreases the effect of lansoprazole

Levofloxacin: Formation of non-absorbable complexes

Levothyroxine: Sucralfate decreases the effect of levothyroxine

Moxifloxacin: Formation of non-absorbable complexes

Norfloxacin: Formation of non-absorbable complexes

Ofloxacin: Formation of non-absorbable complexes

Phenytoin: Sucralfate decreases the effect of hydantoin

Trovafloxacin: Sucralfate may decrease the absorption of orally administered Trovafloxacin. The Sucralfate formulation contains aluminum ions that may intefere with Trovafloxacin absorption. Administer Trovafloxacin 2 hours before or 6 hours after the Sucralfate dose to minimize the interaction.

Warfarin: Sucralfate may reduce the absorption of warfarin. Warfarin should be administered at least 2 hours before or 6 hours after sucralfate administration. Monitor for changes in prothrombin time if sucralfate is initiated, discontinued or dose changed.